Mukund
๐ค SpeakerAppearances Over Time
Podcast Appearances
We had no idea how long the fluid had been in his belly.
If you look at the loculations that were present on ultrasound, I think I would argue that the fluid had been in his belly for quite some time, actually, enough time to develop septations.
And so could the LDH have just been a result of a red blood cell breakdown?
Could the bilirubin in his ascites fluid have been either from ruptured cholecystitis or, again, just a result of RBC breakdown?
I think it's hard to tell.
Even before we started thinking about the etiologies for portal hypertensive versus non-portal hypertensive ascites, we were very confused about how exactly to interpret that peritoneal fluid.
The last thing that I'll bring up here is that the question of does he have cirrhosis or doesn't he have cirrhosis was also a hot topic throughout his admission.
None of us could really justify a reason for him to have cirrhosis except by congestive hepatopathy and long-term hepatic congestion from heart failure.
And ultimately, I think that's what the biopsy showed is that he didn't have frank cirrhosis, but that the changes that we saw in his liver were a result of congestion.
I looked back at all of his data over years and he never had elevated LFTs.
So at most his AST was just above the upper limit of normal.
And I think it's a really interesting presentation of what we ultimately with tissue did decide was congestion.
But that his liver morphology had changed, the contour of his liver had changed to be read in multiple scans as cirrhosis, but without tissue findings compatible with cirrhosis and without LFT elevations compatible with chronic congestion.
Finally, I think I'll just highlight the diagnosis that you guys have invoked many times, which is portosinusoidal venoclusive or vascular disease, which is a rare cause of presinusoidal portal hypertension.
I think you caught exactly that the tension we had was that he didn't have an elevated hepatic venous gradient.
But the gradient measures specifically sinusoidal pressure, not presinusoidal pressure.
So if he had presinusoidal portal hypertension, that could be a falsely depressed gradient.
To add another dimension to this conversation, ascites is specifically a feature of sinusoidal hypertension.
So if you have presinusoidal portal hypertension, classically, you don't even get ascites because the ascites come from the transcapillary leak of the...
ascites fluid from the capillaries of the sinusoidal system.